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Clinical immunology : the official journal of the ... 49건

  1. [해외논문]   The microbiota and autoimmunity: Their role in thyroid autoimmune diseases   SCI SCIE SCOPUS

    Kö (University Hopital Essen, Institute of Medical Microbiology, Essen, Germany ) , hling, Hedda L. (Cultech Ltd., Baglan, Port Talbot, United Kingdom ) , Plummer, Sue F. (School of Biosciences, Cardiff University, Cardiff, United Kingdom ) , Marchesi, Julian R. (Kirkstall Ltd., Templeborough, Rotherham, United Kingdom ) , Davidge, Kelly S. (Division of Infection & Immunity, School of Medicine, Cardiff University, Cardiff, United Kingdom) , Ludgate, Marian
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 63 - 74 , 2017 , 1521-6616 ,

    초록

    Abstract Since the 1970s, the role of infectious diseases in the pathogenesis of Graves' disease (GD) has been an object of intensive research. The last decade has witnessed many studies on Yersinia enterocolitica , Helicobacter pylori and other bacterial organisms and their potential impact on GD. Retrospective, prospective and molecular binding studies have been performed with contrary outcomes. Until now it is not clear whether bacterial infections can trigger autoimmune thyroid disease. Common risk factors for GD (gender, smoking, stress, and pregnancy) reveal profound changes in the bacterial communities of the gut compared to that of healthy controls but a pathogenetic link between GD and dysbiosis has not yet been fully elucidated. Conventional bacterial culture, in vitro models, next generation and high-throughput DNA sequencing are applicable methods to assess the impact of bacteria in disease onset and development. Further studies on the involvement of bacteria in GD are needed and may contribute to the understanding of pathogenetic processes. This review will examine available evidence on the subject. Highlights Graves' disease is an autoimmune condition causing hyperthyroidism. A role for micro-organisms in breaking immune tolerance has been postulated. Recent studies suggest that the gut microbiota may alter the balance between inflammatory/regulatory T cells. This review considers factors which might modify the gut microbiome and methods to assess them.

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  2. [해외논문]   Immunoglobulin and B-cell disturbances in patients with chronic idiopathic neutropenia   SCI SCIE SCOPUS

    Mavroudi, Irene (Department of Hematology, School of Medicine, University of Crete, Greece ) , Eliopoulos, Aristides G. (Molecular and Cellular Biology Laboratory, School of Medicine, University of Crete, Heraklion, Greece ) , Pontikoglou, Charalampos (Department of Hematology, School of Medicine, University of Crete, Greece ) , Pyrovolaki, Katerina (Department of Hematology, School of Medicine, University of Crete, Greece ) , Damianaki, Athina (Department of Hematology, School of Medicine, University of Crete, Greece ) , Koutala, Helen (Department of Hematology, School of Medicine, University of Crete, Greece ) , Zervou, Maria I. (Department of Internal Medicine, School of Medicine, University of Crete, Greece ) , Ximeri, Maria (Department of Hematology, School of Medicine, University of Crete, Greece ) , Mastrodemou, Semeli (Department of Hematology, School of Medicine, University of Crete, Greece ) , Kanellou, Peggy (Department of Hematology, School of Medicine, University of Crete, Greece ) , Goulielmos, George N. (Department of Internal Medicine, School of Medicine, University of Crete, Greece ) , Papadaki, Helen A. (Department of Hematology, School of Medicine, University of Crete, Greece)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 75 - 81 , 2017 , 1521-6616 ,

    초록

    Abstract Chronic idiopathic neutropenia (CIN) is a granulocytic disorder associated with presence of activated, myelosuppressive T-lymphocytes. In the present study we have evaluated constituents of humoral immunity in CIN patients ( n = 48) compared to healthy controls ( n = 52). CIN patients displayed lower serum IgG levels due to a reduction in IgG1, IgG3, IgG4 but not IgG2, lower IgA and increased IgM levels compared to controls. The proportion of CD19 + cells did not differ between patients and controls; however the proportion of the naIve IgD + /CD27 − B-cells was increased and the proportion of class-switched memory IgD − /CD27 + B-cells was decreased in the patients. The percentage of CD40 + B-cells did not differ between patients and controls and no aberrations in the CD40-meadiated signal transduction pathway or in CD40-gene polymorphisms were identified. These data provide further evidence that immune disturbances are associated with the pathophysiology of CIN and point out for the first time the implication of the B-cell system. Highlights Patients with CIN display altered serum immunoglobulin levels. Patients with CIN display increased proportion of naIve IgD + /CD27 − B-cells. Patients with CIN display decreased proportion of class-switched memory IgD − /CD27 + B-cells. The CD40-CD40L expression is normal in CIN. The CD40-meadiated signal transduction pathway is normal in CIN.

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  3. [해외논문]   Dendritic cells activation is associated with sustained virological response to telaprevir treatment of HCV-infected patients   SCI SCIE SCOPUS

    Sacchi, Alessandra (Cellular Immunology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Tumino, Nicola (Cellular Immunology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Turchi, Federica (Cellular Immunology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Refolo, Giulia (Cellular Biology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Fimia, GianMaria (Cellular Biology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Ciccosanti, Fabiola (Cellular Biology Laboratory, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Montalbano, Marzia (Clinical Division, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Lionetti, Raffaella (Clinical Division, “Lazzaro Spallanzani” National Institute for Infectious Diseases, IRCCS, Rome, Italy ) , Taibi, Chiara (Clinical Division, “Lazzaro Spallanzani” Nation) , D'Offizi, Gianpiero , Casetti, Rita , Bordoni, Veronica , Cimini, Eleonora , Martini, Federico , Agrati, Chiara
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 82 - 90 , 2017 , 1521-6616 ,

    초록

    Abstract First anti-HCV treatments, that include protease inhibitors in conjunction with IFN-α and Ribavirin, increase the sustained virological response (SVR) up to 80% in patients infected with HCV genotype 1. The effects of triple therapies on dendritic cell (DC) compartment have not been investigated. In this study we evaluated the effect of telaprevir-based triple therapy on DC phenotype and function, and their possible association with treatment outcome. HCV+ patients eligible for telaprevir-based therapy were enrolled, and circulating DC frequency, phenotype, and function were evaluated by flow-cytometry. The antiviral activity of plasmacytoid DC was also tested. In SVR patients, myeloid DC frequency transiently decreased, and returned to baseline level when telaprevir was stopped. Moreover, an up-regulation of CD80 and CD86 on mDC was observed in SVR patients as well as an improvement of IFN-α production by plasmacytoid DC, able to inhibit in vitro HCV replication. Highlights Decrease of myeloid dendritic cells from SVR HCV+ patients treated with telaprevir Up-regulation of CD80 and CD86 on mDC from SVR during telaprevir treatment Improvement of IFN-α production by pDC, able to inhibit HCV replication

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  4. [해외논문]   Retinoic acid induction of CD1d expression primes chronic lymphocytic leukemia B cells for killing by CD8+ invariant natural killer T cells   SCI SCIE SCOPUS

    Ghnewa, Yasmeen G. (Department of Immunology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland ) , O'Reilly, Vincent P. (Department of Immunology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland ) , Vandenberghe, Elisabeth (Department of Haematology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland ) , Browne, Paul V. (Department of Haematology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland ) , McElligott, Anthony M. (Department of Haematology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland ) , Doherty, Derek G. (Department of Immunology, School of Medicine, Trinity translational Medicine Institute, Trinity College Dublin, Ireland)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 91 - 98 , 2017 , 1521-6616 ,

    초록

    Abstract Invariant natural killer T (iNKT) cells are cytotoxic T cells that respond to glycolipid antigens presented by CD1d. Therapeutic activation of iNKT cells with α-galactosylceramide (α-GalCer) can prevent and reverse tumor growth in mice and clinical trials involving α-GalCer-stimulated iNKT cells are ongoing in humans. B cells express CD1d, however, we show that CD1d expression is reduced on B cells from patients with chronic lymphocytic leukemia (CLL). B cells from CLL patients pulsed with α-GalCer failed to stimulate cytolytic degranulation by iNKT cell lines, but could present the more potent glycolipid analogue, 7DW8-5. Retinoic acid receptor-α (RAR-α) agonists induced CD1d expression by CLL B cells, restoring their ability to present α-GalCer to CD8α + iNKT cells, resulting in cytolytic degranulation. Thus, RAR-α agonists can augment the anti-tumor activities of iNKT cells against CLL cells in vitro . Their inclusion in iNKT cell-based therapies may benefit patients with CLL. Highlights CD1d expression is reduced on B cells from CLL patients. CLL B cells have reduced capacity to present glycolipid antigens to iNKT cells. Retinoic acid induces CD1d expression by CLL B cells. Retinoic acid primes CLL B cells for killing by CD8α + iNKT cells Including retinoic acid in iNKT cell-based therapies may benefit patients with CLL.

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  5. [해외논문]   Adjuvant formulations for virus-like particle (VLP) based vaccines   SCI SCIE SCOPUS

    Cimica, Velasco (TechnoVax, Inc., 765 Old Saw Mill River Road, Tarrytown, NY 10591, United States ) , Galarza, Jose M. (TechnoVax, Inc., 765 Old Saw Mill River Road, Tarrytown, NY 10591, United States)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 99 - 108 , 2017 , 1521-6616 ,

    초록

    Abstract The development of virus-like particle (VLP) technology has had an enormous impact on modern vaccinology. In order to optimize the efficacy and safety of VLP-based vaccines, adjuvants are included in most vaccine formulations. To date, most licensed VLP-based vaccines utilize the classic aluminum adjuvant compositions. Certain challenging pathogens and weak immune responder subjects may require further optimization of the adjuvant formulation to maximize the magnitude and duration of the protective immunity. Indeed, novel classes of adjuvants such as liposomes, agonists of pathogen recognition receptors, polymeric particles, emulsions, cytokines and bacterial toxins, can be used to further improve the immunostimulatory activity of a VLP-based vaccine. This review describes the current advances in adjuvant technology for VLP-based vaccines directed at viral diseases, and discusses the basic principles for designing adjuvant formulations for enhancing the vaccine immunogenicity. Highlights Virus-like particle (VLP) technology has significantly contributed to modern vaccinology. Adjuvant formulation is fundamental for VLP-based vaccines efficacy and safety. Novel classes of adjuvants have been developed for enhancing vaccine immunity. We discuss progress in adjuvant development and formulation for VLP-based vaccines. Advances in these fields should bring forward more effective and safer vaccines. Graphical abstract The roles of adjuvants in VLP-based vaccines. VLPs can be produced from various cellular systems using recombinant DNA technology. Adjuvants play multiple roles in enhancing the efficacy and safety of VLP-based vaccines. [DISPLAY OMISSION]

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  6. [해외논문]   Large BTK gene mutation in a child with X-linked agammaglobulinemia and polyarthritis   SCI SCIE SCOPUS

    Sharma, Dhrubajyoti (Corresponding author.) , Gupta, Aman , Goel, Shubham , Sharma, Madhubala , Rawat, Amit , Singh, Surjit
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 109 - 111 , 2017 , 1521-6616 ,

    초록

    Highlights Polyarthritis as presenting feature in patients with XLA is extremely uncommon. A novel mutation in BTK gene is described. Regular replacement IVIG results in resolution of arthritis in patients with XLA.

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  7. [해외논문]   Maternal T and B cell engraftment in two cases of X-linked severe combined immunodeficiency with IgG1 gammopathy   SCI SCIE SCOPUS

    Okano, Tsubasa (Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan ) , Nishikawa, Takuro (Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan ) , Watanabe, Eri (Laboratory of Diagnostic Medicine, Institute of Medical Science, The University of Tokyo, Tokyo, Japan ) , Watanabe, Takashi (Laboratory for Integrative Genomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan ) , Takashima, Takehiro (Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan ) , Yeh, Tzu-Wen (Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan ) , Yamashita, Motoi (Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan ) , Tanaka-Kubota, Mari (Department of Pediatrics and Developmental) , Miyamoto, Satoshi , Mitsuiki, Noriko , Takagi, Masatoshi , Kawano, Yoshifumi , Mochizuki, Yoshiki , Imai, Kohsuke , Kanegane, Hirokazu , Morio, Tomohiro
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 112 - 120 , 2017 , 1521-6616 ,

    초록

    Abstract X-linked severe combined immunodeficiency (X-SCID), caused by defects in the common gamma chain, is typically characterized by T and NK cell defects with the presence of B cells. T cell dysfunction and impaired class-switch recombination of B cells mean that patients typically have defects in class-switched immunoglobulins (IgG, IgA, and IgE) with detectable IgM. Here, we describe two patients with X-SCID with IgG1 gammopathy, in whom we identified maternal T and B cell engraftment. Exclusively, maternal B cells were found among the IgD − CD27 + class-switched memory B cells, whereas the patients' B cells remained naIve. In vitro stimulation with CD40L+IL-21 revealed that peripheral blood cells from both patients produced only IgG1. Class-switched maternal B cells had restricted receptor repertoires with various constant regions and few somatic hypermutations. In conclusion, engrafted maternal B cells underwent class-switch recombination and produced immunoglobulin, causing hypergammaglobulinemia in patients with X-SCID. Highlights Two cases of atypical X-SCID with IgG1 gammopathy had maternal T and B cell engraftment. Only maternal B cells differentiated to class-switched memory B cells and produced IgG1. Pre-class switched B cells engrafted then underwent class switch recombination in SCID patients. This is the first report to identify maternal B cell engraftment in B + SCID.

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  8. [해외논문]   IFNA-AS1 regulates CD4+ T cell activation in myasthenia gravis though HLA-DRB1   SCI SCIE SCOPUS

    Luo, Mengchuan (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Liu, Xiaofang (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Meng, Huanyu (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Xu, Liqun (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Li, Yi (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Li, Zhibin (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Liu, Chang (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Luo, Yue-Bei (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Hu, Bo (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China ) , Xue, Yuanyuan (Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008) , Liu, Yu , Luo, Zhaohui , Yang, Huan
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 121 - 131 , 2017 , 1521-6616 ,

    초록

    Abstract Abnormal CD4 + T cell activation is known to play roles in the pathogenesis of myasthenia gravis (MG). However, little is known about the mechanisms underlying the roles of lncRNAs in regulating CD4 + T cell. In this study, we discovered that the lncRNA IFNG-AS1 is abnormally expressed in MG patients associated with quantitative myasthenia gravis (QMG) and the positive anti-AchR Ab levels patients. IFNG-AS1 influenced Th1/Treg cell proliferation and regulated the expression levels of their transcription factors in an experimental autoimmune myasthenia gravis (EAMG)model. IFNG-AS1 could reduce the expression of HLA-DRB and HLA-DOB and they had a negative correlation in MG. Furthermore IFNG-AS1 influenced the expression levels of CD40L and CD4 + T cells activation in MG patient partly depend on effecting the HLA-DRB1 expression. It suggests that IFNG-AS1 may be involved in CD4 + T cell-mediated immune responses in MG. Highlights IFNG-AS1 decreased Th1, promoted Treg cell proliferation and influenced the expression levels of their transcription factors in EAMG model. IFNG-AS1 reduced the expression levels of CD40L and TF T-bet in CD4 + T cells of MG patient. IFNG-AS1 downregulated CD40L and the transcription factor T-bet partly depend on effecting the HLA-DRB1 expression.

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  9. [해외논문]   Complete knockout of estrogen receptor alpha is not directly protective in murine lupus   SCI SCIE SCOPUS

    Scott, Jennifer L. (Medical University of South Carolina, Division of Rheumatology and Immunology, Charleston, SC 29425, USA ) , Wirth, Jena R. (Medical University of South Carolina, Division of Rheumatology and Immunology, Charleston, SC 29425, USA ) , Eudaly, Jackie (Medical University of South Carolina, Division of Rheumatology and Immunology, Charleston, SC 29425, USA ) , Ruiz, Phil (University of Miami, School of Medicine, Department of Pathology, 1611 N.W. 12th Ave., Holtz Center, East Tower, Room 2101, Miami, FL 33136, USA ) , Cunningham, Melissa A. (Medical University of South Carolina, Division of Rheumatology and Immunology, Charleston, SC 29425, USA)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 132 - 141 , 2017 , 1521-6616 ,

    초록

    Abstract Systemic lupus erythematosus (SLE) is a chronic and potentially severe autoimmune disease that disproportionately affects women. Despite a known role for hormonal factors impacting autoimmunity and disease pathogenesis, the specific mechanisms of action remain poorly understood. Our laboratory previously backcrossed “estrogen receptor alpha knockout (ERαKO)” mice onto the NZM2410 lupus prone background to generate NZM/ERαKO mice. This original ERαKO mouse, developed in the mid-1990s and utilized in hundreds of published studies, is not in fact ERα null. They express an N-terminally truncated ERα, and are considered a functional KO. They have physiologic deficiencies including infertility due to disruption of a critical activation domain (AF-1) at the N terminus of ERα, required for most classic estrogen (E2) actions. We demonstrated that female NZM/ERαKO mice had significantly less renal disease and significantly prolonged survival compared to WT littermates despite similar serum levels of autoantibodies and glomerular immune complex deposition. Herein, we present results of experiments using a lupus prone true ERα−/− mice (deletional KO mice on the NZM2410 background), surprisingly finding that these animals were not protected if they were ovariectomized, suggesting that another hormonal component confers protection, possibly testosterone, rather than the absence of the full-length ERα. Highlights NZM2410 ERα−/− mice are not protected from lupus disease expression if ovariectomized. ERα disruption increases, not decreases, autoantibody production in the NZM2410 model. E2 can exacerbate lupus disease expression via a mechanism that is independent of ERα. DCs & their subsets (cDC1, cDC2) are not altered by E2 or ERα on the NZM background.

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  10. [해외논문]   Combined immunodeficiency with EBV positive B cell lymphoma and epidermodysplasia verruciformis due to a novel homozygous mutation in RASGRP1   SCI SCIE SCOPUS

    Platt, Craig D. (Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Fried, Ari J. (Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Hoyos-Bachiloglu, Rodrigo (Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Usmani, G. Naheed (Division of Pediatric Hematology and Oncology, University of Massachusetts Medical Center, Worcester, MA, United States ) , Schmidt, Birgitta (Department of Pathology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Whangbo, Jennifer (Division of Hematology-Oncology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Chiarle, Roberto (Department of Pathology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Chou, Janet (Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States ) , Geha, Raif S. (Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 142 - 144 , 2017 , 1521-6616 ,

    초록

    Abstract RASGRP1 is a guanine-nucleotide-exchange factor essential for MAP-kinase mediated signaling in lymphocytes. We report the second case of RASGRP1 deficiency in a patient with a homozygous nonsense mutation in the catalytic domain of the protein. The patient had epidermodysplasia verruciformis, suggesting a clinically important intrinsic T cell function defect. Like the previously described patient, our proband also presented with CD4 + T cell lymphopenia, impaired T cell proliferation to mitogens and antigens, reduced NK cell function, and EBV-associated lymphoma. The severity of the disease and the development of EBV lymphoma in both patients suggest that hematopoietic stem cell transplantation should be performed rapidly in patients with RASGRP1 deficiency. Highlights We report the second known case of deficiency of RASGRP1 deficiency. RASGRP1 is essential for MAP-kinase mediated signaling in lymphocytes. Patients with RASGRP1 deficiency present with a combined immunodeficiency. These patients have increased susceptibility to EBV-driven lymphoma.

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